Objective. Previous studies have yielded conflicting results regarding the association of coronavirus disease 2019 (COVID‐19) with allergic rhinitis (AR). Data on AR prevalence in COVID‐19 patients are limited. Consequently, whether AR is a harmful or protective factor for COVID‐19 patients remains controversial. Therefore, we analyzed the relationship between COVID‐19 and AR. Methods. We systematically searched PubMed, Embase, Cochrane, and Web of Science databases for studies published between January 1, 2020 and January 11, 2022. We included studies reporting the epidemiological and clinical characteristics of COVID‐19 and its incidence in patients with AR. We excluded letters, case reports, literature review articles, non‐English language article, and non‐full‐text articles. The raw data from these studies were pooled into a meta‐analysis. Results. We analyzed the results of nine studies. The prevalence of AR in patients with COVID‐19 was 0.13 (95% confidence interval [CI] 0.04–0.25), with an overall I² of 99.77%, P = 0.24. COVID‐19 patients with AR are less prone to severe disease (odds ratio [OR] = 0.79, 95% CI, 0.52–1.18, P = 0.25) and hospitalization (OR = 0.23, 95%CI, 0.02–2.67, P ≤ 0.0001) than patients without AR. Conclusion. Our data suggest that allergic rhinitis is a protective factor in patients with COVID‐19.

Background: This study aims to compare the effectiveness and safety of enhanced recovery after surgery (ERAS) in patients with hepatocellular carcinoma (HCC) undergoing hemihepatectomy. Methods: From January 2017 to June 2019, 54 and 56 patients were enrolled into the control and ERAS group, retrospectively. All the indicators related to operation, liver functions, and postoperative outcomes were included in the analysis. Propensity score matching (PSM) analysis identified 72 patients for further analysis. Results: The clinicopathological characteristics were well-matched after PSM, and there were no significant differences in the operative duration, blood loss, blood transfusion, hospital costs, and most postoperative indicators in these 2 groups. In the ERAS group, D-dimer and fibrin degradation product values were significantly reduced (3.57 (2.874.60) μg/ml vs 4.81 (3.948.29) μg/ml and 11.90 (10.0418.02) μg/ml vs 15.80 (11.5529.24) μg/ml; P = .002 and P = .023, respectively). The days that semiliquid diet was allowed after surgery (2.00 (2.003.00) days vs 5.00 (4.006.00) days, P < .001), abdominal drainage tube indwelling duration (5.00 (4.005.00) days vs 5.00 (4.756.25) days, P = .004), and hospital stay after surgery (6.00 (6.007.00) days vs 8.00 (7.0010.00) days, P < .001) were also significantly shorter. The proportion of patients requiring analgesic treatment was significantly lower in the postoperative day 2 and day 4 ( P < .001 and P = .025, respectively). The morbidity was significantly less (36.11% vs 69.44%, P = .005). Conclusions: ERAS programs are feasible and safe in HCC patients undergoing hemihepatectomy. Postoperative anticoagulant therapy may be one of the necessary steps.

Inflammation plays an important role in age‐related hearing loss (ARHL). Transforming growth factor‐β‐activated protein 1 (TAK1), a key factor upstream of inflammatory pathways, mediates various cell death pathways, potentially influencing the survival and death of cochlear hair cells. The DBA/2 J mouse model and the HEI‐OC1 cell line were used to investigate the mechanism of TAK1‐mediated inflammation in ARHL. Hematoxylin and eosin staining revealed significant histological damage in the cochlea of 16‐week‐old mice, along with an increase in auditory‐evoked brainstem response thresholds. Concurrently, TAK1 mRNA levels decreased sharply, and necroptosis significantly increased in 16‐week‐old mice, indicating a correlation between TAK1 expression, necroptosis, and hearing loss. We subsequently constructed TAK1 knockdown and overexpression HEI‐OC1 cells for further investigation. TAK1 knockdown in HEI‐OC1 cells significantly activated the necroptotic pathway, characterized by an increase in necroptosis, along with up‐regulation of RIPK3 and MLKL , and down‐regulation of NF‐κB and Caspase 8 . However, TAK1 overexpression successfully prevented necroptosis in HEI‐OC1 cells, leading to decreases in NF‐κB , Caspase 8 , RIPK3 , and MLKL . We further treated TAK1 knockdown cells with necroptosis inhibitors and found that they could reverse the damage caused by TAK1 knockdown in HEI‐OC1 cells. This preliminary study shows that TAK1‐mediated necroptotic pathways play an important role in the pathogenesis of ARHL.